More Recent Comments

Saturday, January 07, 2012

Should Undergraduates Study the Primary Scientific Literature?

 
The short answer to the question posed in the title is "yes" but there are many caveats. One of them is that it depends on what level you are teaching. In my opinion, the value of exposing science students to the primary scientific literature (papers) increases as students progress from first year to the year they graduate. Students in their final year of a science program will gain a lot from being exposed correctly to the scientific literature but students in introductory course will hardly benefit at all—and may, in fact, be harmed if it takes time away from learning basic principles and concepts.

It is important to teach critical thinking and it's important to focus education on basic principles and concepts. Most of the basic principles and concepts in a discipline have been developed over several decades. The work that led to those ideas is (usually) in the primary scientific literature but you can't learn the concept by just reading a few key papers. Evolution is a good example but so is our understanding of how cells generate energy from proton gradients, how enzymes work, and how the information in messenger RNA gets translated into proteins.

I find it helpful to remind myself from time to time that the vast majority of the students I teach will never be scientists and many of them aren't really interested in how to do scientific experiments. They will become average citizens in all kinds of careers that have nothing to do with the basic sciences. Our goal is to make them scientifically literate so they will understand why evolution is true, why homeopathy is bunkum, why they should vaccinate their children, and why humans are behind global climate change. I don't think we can achieve that goal by focusing on the primary scientific literature, especially in the early years of undergraduate education.

C.R.E.A.T.E. is a education project funded by the United States National Science Foundation (Grant No. 1021443). It's goal is "transform understanding of science" by using the primary scientific literature as a teaching tool. Here's how they describe their approach ...
The C.R.E.A.T.E. (Consider, Read, Elucidate the hypotheses, Analyze and interpret the data, and Think of the next Experiment) method is a new teaching approach that uses intensive analysis of primary literature to demystify and humanize research science for undergraduates. Our goal is to use the real language of science—the journal article—as an inroad to understanding “who does science, how, and why?” At the same time, we wish to help students (1) experience authentic processes of science, in particular discussion/debate about experimental data and their interpretation (including ‘grey areas’), (2) recognize the creativity and open-ended nature of research, and (3) see the diversity of people who undertake research careers (i.e. not just the genius/geeks of popular culture). As a complement to teaching based on textbooks, which tend to oversimplify the research process, C.R.E.A.T.E. teaching focuses on on authentic published work--peer reviewed journal articles—with students reading either series of papers produced sequentially from individual labs or series of papers from different labs focused on a single line of research.

By reading/analyzing a set of papers published in series from a single lab, students experience the evolution of research projects over a period of years. Using newly-developed C.R.E.A.T.E. pedagogical tools, that encourage multiple approaches to the material (concept mapping, sketching, visualization, transformation of data, creative experimental design) students gain deep understanding of the methods (and biological content/principles) that underlie each individual experiment of the paper. In class, we emphasize scientific thinking--focusing on understanding both why and how each part of the study was done, by examining the hypotheses underlying each aspect of the study, and analyzing/discussing the data represented in each figure and table. Students learn to interpret complex data, draw conclusions, debate interpretations, and re-represent data (e.g. represent tabled data in graphic form) to aid understanding. Content knowledge is reviewed as students consider the principles underlying the techniques used, as well as the overall context of the scientific question being addressed (e.g. a module focused on regeneration would likely include review multiple aspects of cell division, cell differentiation, gene expression and stem cells, drawing on information students learned in other classes and helping them to apply it in a real-world research situation). C.R.E.A.T.E. students thus learn a variety of transferable learning skills that can be applied to complex scientific reading they do in the future. Students design their own proposed followup experiments at several points in the semester, and debate each other’s proposed studies in a classroom exercise modeled on activities of bona fide scientific grant panels. Such discussions reveal the research process to be openended, with multiple branch points or possible “next directions to go;” thus much less linear and predictable than many students expect. Late in the process, students generate a short list of questions for paper authors that are sent as an email survey to each author (not simply the PI). Responses from multiple authors provide unique behind-the-scenes insight into “the people behind the papers,” humanizing the research experience and showing researchers to be complex individuals much like the students themselves.
Here's an example based on Pattern formation during regeneration in planaria.

This is an approach that views experiment as the primary focus of science whereas I tend to see science as a much broader way of knowing. The C.R.E.A.T.E. approach to undergraduate education emphasizes the doing of science rather than the understanding of the results and how they fit into a bigger picture. It probably does a good job of looking at "trees" but not so good a job when it comes to seeing the "forest."

I don't know the correct balance between teaching principles, ideas, and concepts and teaching the experimental approach taken by actual research scientists in their day-to-day activities. There's no question that lab courses are extremely important but I'm quite skeptical about bringing the study of experimental techniques into the lecture courses if it take time away from the conceptual understanding of the discipline.


[Hat Tip: Sandra Porter at Discovering Biology in a Digital World: Learn how to use scientific articles in education at the C.R.E.A.T.E. June workshop]

Chris Hogue on Complexity and Evolution

 
Chris Hogue is a Canadian biochemist/bioinformatician who works on protein folding (among other things) at the National University of Singapore. He used to be a professor in my department here at the University of Toronto. I miss him, and wish he were still here.

Chris blogs at BioImplement and he has just started a new series of posts on Complexity and Evolution. His goal is to explain how human design can inform us about evolution. The idea is to refute the arguments of Intelligent Design Creationists who treat intelligent design as something mystical that's1 beyond naturalism.

Here's how Chris explains what's coming ...
The thread connecting these examples of human design is that each one is an analogy to biological evolution, from which evolution may be better understood by laypersons. Now by posting new examples like this, I realize that they may all be stolen by the “intelligent design” (ID) creationists to argue against evolution. My view on ID follows that most clearly expressed in the 2005 court judgment from the Pennsylvania Kitzmiller v. Dover case: “The overwhelming evidence at trial established that ID is a religious view, a mere re-labeling of creationism, and not a scientific theory.” Of course a few scientists have written in defense of evolution and against ID nonsense in the classroom, the most strident of whom is Richard Dawkins. I now add my voice in support, as in his final interview with Dawkins, Christopher Hitchens lamented “It’s the shame of your colleagues that they don’t form ranks and say, ‘Listen, we’re going to defend our colleagues from these appalling and obfuscating elements.’”

So into the breach, I add my voice with some new arguments, after this small bit of throat-clearing. I will try to avoid being derivative as I come armed with my own capacity for inquiry, insight, and argument. My examples will show how ID concepts force the gerrymandering of human design history, and surround it with mystical borders to make their claims. The individual steps in human design are small, slow and absolutely require the intellectual imprinting of lessons by trial and error. Students who are led to think falsely about human design, or any complexity as having mystical origins are harmed by the diminishment of their own aspirations of creativity. We all need to understand how small steps and tools lead to human creativity and any object of complexity. I will reveal these small steps and show, where I can, the failures that led to success.
I know Chris and I can assure you that his upcoming posts will be provocative and informative.




Friday, January 06, 2012

Plant microRNAs in Your Blood?

 
Last month the science magazines and websites were all talking about a paper by Zhang et al. (2012) published in Cell Research. These workers discovered plant micoRNAs in the serum of mice and humans. The microRNAs seem to come from ingested rice. Presumably the micoRNAs are taken up in the intestine and secreted into the blood in small vesicles. The concentration of the major rice miRNAs in serum is about 10 fM or 10×10-15 moles per liter.1

The authors have shown that microRNA MI168a binds to the mRNA of low-density lipoprotein receptor adapter protein 1, inhibiting translation. This leads to the idea that ingested plant microRNAs can regulate the expression of human genes. That's the story that generated the most press [What You Eat Affects Your Genes: RNA from Rice Can Survive Digestion and Alter Gene Expression, Food We Eat Might Control Our Genes].

This is one of those findings where the explanation doesn't make a lot of sense but the data seem sound. It seems very unlikely that small plant RNAs could survive the processing and digestion of rice or any other food and even less likely that they would find their way into the bloodstream where they could play a role in regulating mammalian gene expression. I think I'll wait for confirmation.

It's a shame that none of the articles in the popular press expressed any sort of skepticism. That's one of the problems with science journalism. How do you convey the idea that all scientific results are preliminary until they have been confirmed by others?


1. That concentration is far below the concentration where effective binding can occur but the idea seems to be that the micoRNAs are contained in small vesicles that subsequently fuse with liver cells and deliver the rice microRNA to the cytoplasm where it can inhibit translation of specific mammalian RNAs. It's difficult to see how one could get an effective concentration of plant microRNA in one of these mammalian cells.

Zhang, L., Hou, D., Chen, X., Li, D., Zhu, L., Zhang, Y., Li, J., Bian, Z., Liang, X., Cai, X., Yin, Y., Wang, C., Zhang, T., Zhu, D., Zhang, D., Xu, J., Chen, Q., Ba, Y., Liu, J., Wang, Q., Chen, J., Wang, J., Wang, M., Zhang, Q., Zhang, J., Zen, K., and Zhang, CY. (2012) Exogenous plant MIR168a specifically targets mammalian LDLRAP1: evidence of cross-kingdom regulation by microRNA. Cell Research 22:107–126 [PubMed] [doi:10.1038/cr.2011.158]

An important correction to several of the figures in this paper has also been published.

Zhang et al. (2012) Corrigendum [doi:10.1038/cr.2011.174]


Carnival of Evolution #43

 
This month's Carnival of Evolution (43rd version) is hosted by The EEB & Flow, a blog written by a large group of people interested in evolution and ecology [Carnival of Evolution #43]. The post was written by Marc Cadotte [Cadotte Lab], a professor in the Department of Evolution & Ecology right here at the University of Toronto.
You no longer need to ponder the mysteries of life, travel the globe making observations, or running complex experiments to test hypotheses; everything you want to know about evolution today can be found by reading the monthly installments of the Carnival of Evolution!

The first installment of 2012 (or is this the last of 2011?) offers a great smattering of many different aspects of current evolutionary understanding. These 26 posts cover many of the major areas of research that define current evolutionary biology.

The next Carnival of Evolution (February) needs a host. Contact Bjørn Østman at Carnival of Evolution if you want to volunteer. Meanwhile, you can submit your articles for next month's carnival at Carnival of Evolution.


Sunday, December 25, 2011

And the Winner Is .....

 
I collected the names of all the undergraduates who got the right answer for Monday's Molecules. I put them on slips of paper and had my colleague, Alex Palazzo draw one of them from a small beaker.

Alex still has a blog on Scienceblogs called Transcription and Translation (formerly The Daily Transcript) but he hasn't blogged very much recently. He's too busy doing experiments.

What name did he draw out of the beaker?

The winner of a free autographed textbook is .....

Thursday, December 22, 2011

The Cambrian Conundrum: Fossils vs Genes

The earliest fossil examples of most animal classes and phyla appear in the fossil record at about the same time in the Cambrian (about 530 million year as ago (Ma)). This period of apparent rapid divergence is referred to as the "Cambrian Explosion."

It seemed unlikely that this disparity could have evolved in just a few million years so many scientists have been searching for fossil antecedents in the early Cambrian and Ediacaran (635-541 Ma). Many trace fossils have been found in the past few decades, indicating that the fossil animals of the Cambrian were preceded by small wormlike creatures.

The other approach has been sequence analysis. One can construct molecular phylogenies by comparing the sequences of genes in modern extant organisms. This approach has been highly successful over the past fifty years so that we now know a great deal about the relationship of the various animal phyla. The correspondence between the old morphological taxonomy and molecular evolution is the most powerful evidence we have that evolution explains the history of life [see Twin Nested Hierarchies].

The problem with sequence comparisons has always been getting accurate dates using the molecular clock. It is hard to get an accurate date when dealing with events that occurred 500 million years ago because there aren't very many calibration points. An accurate calibration point is a known time when two lineages diverge.

If there really was a rapid divergence in the Cambrian then one would expect the molecular tree to show this. But it never has. The molecular phylogeny shows that chordates diverged from invertebrates at least one hundred million years before their fossils appear in the Cambrian. Similarly other phyla and classes of animals have their origin long before the Cambrian, according to the molecular clock.

A recent paper in Science extends this comparison by calculating more a more accurate molecular phylogeny using seven housekeeping genes from 118 different species (Erwin et al. 2011). The result is shown in Figure 1 of the paper: "The origin and diversification of animals as inferred from the geologic and genetic fossil records." (Click on the figure to embiggen.)

Do the IDiots Understand Biochemistry and Molecular Biology?

 
We've been discussing whether Intelligent Design Creationists understand enough about biochemistry, molecular biology, and evolution to warrant their criticisms of these fields. The answer is clearly "no" as they demonstrate time and time again.

This time it's an anonymous posting on the premier IDC website, Evolution News & Views [Long Non-coding RNA Punches Another Hole in "Junk Genome" Myth]. The anonymous poster links to a recent paper in Genes & Development that shows a function for a particular long non-coding (lnc) RNA. The paper implies that many of these lncRNAs (up to 400) are expressed in mouse erythroid cells.

Regulatory RNA have been known and studied for at least four decades and various lncRNAs have been characterized over the past twenty years. The IDiot at Evolution News & Views seems to think that this is a new discovery proving that there's no junk in our genome. The facts are quite different.

As I pointed out in my review of The Myth of Junk DNA, the amount of the genome devoted to producing lncRNAs is about 0.1% [Junk & Jonathan: Part 6—Chapter 3]. So, not only have we known about regulatory RNAs for many years, we also know that their genes don't account for very much of the genome, I figure it can't be more than 2% even when you include all of the most optimistic estimates of regulatory RNAs [see What's in Your Genome?].

But the ignorance of the IDiots is much more profound than just being incapable of calculating percentages. The latest posting reveals the depth of their ignorance.
These findings have two important implications. First, non-coding regions of the genome were assumed to be leftover evolutionary relics that no longer play a functional role. The assumption was not due to extensive studies of non-coding regions of the genome, but rather to a commitment to what is known as the central dogma of molecular biology: DNA is transcribed into RNA and RNA is translated into amino acids to make proteins. This was considered the primary purpose of DNA. The non-coding regions were assumed to have no function, and were dismissed as the natural consequence of genetic "junk" accumulating over time. This paper is one among an accumulating corpus of papers discussing new and interesting functions of the non-coding regions of the genome. (See The Myth of Junk DNA by Jonathan Wells for a history of "junk" DNA and additional references describing the function of so-called "junk" DNA. See here for a discussion on the regulatory role of introns.)
There was never a time in the past fifty years when knowledgeable biochemists and molecular biologists thought that all non-coding DNA was nonfunctional junk. This was never an assumption of the Central Dogma of Molecular Biology which states that "... once (sequential) information has passed into protein it cannot get out again" [Basic Concepts: The Central Dogma of Molecular Biology]. There are many scientists who have misconceptions about the Central Dogma [The Central Dogma Strawman] but the IDiots go one step farther by misunderstanding the misconception!

We've known about functions in non-coding DNA since the early 1960s as anyone who has ever glanced at a textbook would know. It's hard to tell whether the IDiots are just butt-ignorant of basic science or whether they are lying. This is an especially tricky problem when the silly strawman argument is popularized by Jonathan Wells because he's supposed to know the science [Junk & Jonathan: Part 1—Getting the History Correct] [Junk & Jonathan: Part 2— What Did Biologists Really Say About Junk DNA?].

We know that most of our genome is junk because we know a great deal about genomes, genes, biochemistry, molecular biology, and evolution. We know which parts are likely to be functional and which parts are likely to be broken genes and other kinds of junk. We know this because we understand the subject, not because we are covering up our ignorance.

The IDiots are ignorant of the science and they assume that everyone else is as well. That's a very bad assumption.


Wednesday, December 21, 2011

Center for Inquiry Canada: New Associate Members

 
The Board of Directors voted on accepting new Associate Members at its December 11th meeting. I have just received a letter from the Board signed by the new (?) Chair, Richard Thain.
Dear Professor Moran,

On December 11, 2011 one of the many important items on the agenda for the Board od Directors meeting was discussion of the applications for Associate Membership.

The goal is to have a diverse group of Associate Members which reflects our membership geographically. In order to achieve this, the Board recognizes that we must update our website and post the By-Laws which explain the governance of CFI Canada. We hope to attract more applications which will then be reviewed before the next CFI Canada AGM in March 2012.

We felt it was important to approve some of the applications at the December 11th board meeting, so we reviewed and accepted the following five people:

Iain Martel, Seanna Watson, Brian Eelhart, Craig Irving and Marlowe Filippov.

The other applications were put under review and will be considered with the next wave of applicants at a future board meeting.

The Board of Directors realizes you have made and are continuing to make significant contributions to our success. We would like to sincerely thank you for your continued support and committment to helping CFI build a better Canada through reason.

Richard Thain DDS
Chair, Board of Directors
CFI Canada
My application was rejected!

I wish I knew why the Board didn't accept my application but did accept some others. Iain Martel is the Chair of CASS and Seanna Watson is the Director of the Ottawa branch of CFI so I assume that the people filling these positions are a sort of ex officio Associate Members. That makes a lot of sense especially for Iain and Seanne who have devoted so much time and effort to CFI.

Bryan Eelhart was the Financial Agent for the Green Party in the riding of Trinity-Spadina (Toronto) during the recent Ontario election. He's a member of the Board of Directors at Conscience Canada and he works for Science for Peace. Bryan has extensive expertise in website design and implementation.

Craig Irving is a freelance videographer from Toronto. He serves on the Multimedia Committee at Centre for Inquiry Canada.

Marlowe Filippov lives in Ottawa where she volunteers at the Centre for Inquiry. She's also an expert in websites. She's been helping out with membership problems and advising the National Director on other issues.

It appears that three two of the new Associate Members were chosen for their ability to help out with updating the CFI website.

There are currently three Associate Members who are CFI Advisory Fellows; Jeff Rosenthal from Toronto, Chris diCarlo from Guelph, and Ethan Clow from Vancouver. It's possible that the Board of Directors felt that only three CFI Canada Advisory Fellows should also be Associate Members, or maybe they felt that having two from the Toronto area was too much and that's why my application was rejected.

I'll try and find out more about the qualifications required for Associate Membership. It's clear that length of membership in CFI is not important since there are Associate Members who only joined CFI two years ago. I think that active volunteering on administrative tasks is an important criterion so if you are currently helping out in this area you will probably have a good chance of being appointed.

I'm a little unclear about the criterion of reflecting membership geographically. About half of all CFI Canada members are from the Toronto area but I don't think this means that half of the Associate Members will be from Toronto. I think it means that you're more likely to be chosen as an Associate Member if you are from one of the other centres that isn't already represented.

I'm not sure what the role of a CFI Canada Advisory Fellows is supposed to be. If we can't be Associate Members then who are we supposed to advise? :-)

Post a comment if your application was also rejected. That way we might be able to figure out what the Board of Directors is thinking when it comes to appointing new Associate Members. I'll let the Board know about this posting so they can comment, or at least see your comments.


A Torley Defense of Irreducible Complexity

Vincent Joseph Torley (vjtorley) has a Ph.D. in Philosophy (2007) from the University of Melbourne (Australia). He currently teaches English in Japan.

Torley hangs out at Uncommon Descent where he tries to defend Intelligent Design Creationism. He didn't like my recent posting on Irreducible Complexity [Barry Arrington Explains Irreducible Complexity] because I accused Barry Arrington of not understanding evolution. You might recall that Arrington began his defense of irreducible complexity by saying, "(1) By definition, evolution can work only in a stepwise fashion wherein each successive step is “selected for” because it has conferred a selective advantage on the organism."

This is not how evolution is defined and it's a particularly bad way to begin because the scientific understanding of many irreducibly complex systems involves the fixation of neutral or even detrimental alleles. Competency in evolution also requires an understanding of redundancy, contingency, and sloppiness.

Vincent Joseph Torley asks, "Will this do, Professor Moran?" He starts with ....
Let me state up-front that I am a philosopher, not a scientist. However, I believe in arguing rigorously, so I have attempted to state the argument from irreducible complexity in a rigorous fashion. I’d appreciate hearing from Professor Moran thinks of this argument, as a biologist.

Tuesday, December 20, 2011

These are not berries!

 

This is Juniperus communis from Botany Photograph of the Day. If you visit that website you'll learn two three things about juniper that you didn't know before: (1) juniper grows in lots of places, (2) the "berries" aren't berries, (3) gin comes from the French word for juniper.


The Mite Genome

 
The genome of the two-spotted spider mite, Tetranychus urticae has been sequenced and the results were published in Nature last month (Grbic et al. 2011).

Spider mites eat plants. They produce silk-like webs and that's why they're called "spider mites". They belong to the class Arachnida, which is the same group that contains spiders. The Arachnids are in the subphylum Chelicerata, a large group of arthropods distantly related to the insects and crustaceans. This is the first genome sequence of a chelicerate and that's why it's important.

Genome Size

The genome is only 90 Mb in size. It's the smallest arthropod genome that has been sequenced so far. Contrast this size with the human genome at 3,200 Mb or the genome of another tick, Ixodes scapularis, estimated to be 2,100 Mb. (Honeybee = 236 Mb, Drosophila = 140 Mb.) According to Ryan Gregory's animal genome size database this is the smallest known arachnid genome and the smallest known arthropod genome.

The authors estimate that there are 18,414 protein-encoding genes in the mite genome. This is about the same number of genes as most insects whose genomes have been sequenced and only slightly less than the number of genes in the human genome.

About 41% of the mite genome consists of exons (protein-encoding). Recall that less than 2% of our genome encodes proteins and in most insects the exon sequences make up less than 10% of the genome. (Honeybees and Drosophila also have smaller than average genome sizes.)

Introns

As you might imagine, the mite genome has a lot less junk DNA than other animals. This is partially reflected in the number and size of the introns. The average protein-encoding gene has less than three introns and the ones that are present are a lot smaller than the introns in species with larger genomes.

The figure on the right is a truncated version of a figure that appears in the supplemental information. It shows that the smallest introns are 40 bp and 70% of all introns are less that 150 bp in length (median = 96 bp). This is close to the smallest possible intron size allowing for slices sites and formation of a loop during splicing.

Transposons and Repetitive Sequences

Transposons (active and degenerate) make up less than 10% of the T. urticae genome and highly repetitive sequences (microsatellites) are almost absent. (The spider mite chromosomes don't have centromeres.)

Transposon sequences and highly repetitive sequences are a major component of the junk DNA found in large genomes so their absence in the mite genome is not a surprise.

Why Is the Mite Genome So Small?

The short answer is, we don't know. The long answer is much more complicated. As Michael Lynch points out (Lynch 2007 p.37), there's a balance between rates of insertion and deletion mutations. In species with small genomes the spontaneous rate of nucleotide deletion exceeds that of insertion so genome sizes shrink over time.

There may not be a selective advantage to having small or large genomes. It may just be that in some species the repair machinery tends to favor deletions while in closely related species the enzymes don't have this bias. Or maybe large genomes are slightly deleterious but the population size isn't large enough to allow natural selection to act. Some lineages may never have encountered significant bottlenecks so they've maintained a huge population size for millions of years allowing natural selection to operate on slightly deleterious mutations. This leads to smaller genomes.

Whatever the explanation, the small genome of mites shows us that most of the junk DNA present in other arthropod genomes is dispensable. That's why it's called "junk."



Grbic, M. et al. (2011) The genome of Tetranychus urticae reveals herbivorus pest adaptations. Nature 479:487-492. [doi: 10.1038/nature10640] [PubMed]

Lynch, M. (2007) "The Origins of Genome Architecture" Sinauer Associates, Inc. Publishers, Sunderland, Massachusetts, United States

Monday, December 19, 2011

Jonathan McLatchie and Junk DNA

 
THEME

Genomes & Junk DNA
Jonathan McLatchie takes on PZ Myers in a spirited attack on junk DNA [Treasure in the Genetic Goldmine: PZ Myers Fails on "Junk DNA"]. The Intelligent Design Creationists are convinced that most of our genome is functional because that's what a good designer would create. They claim that junk DNA is a myth and their "evidence" is selective quotations from the scientific literature. They ignore the big picture, as they so often due.

I discussed most of the creationist arguments in my review of The Myth of Junk DNA.

Jonathan McLatchie analyzes three argument made by PZ Myers in his presentation at Skepticon IV. In that talk PZ said that introns are junk, telomeres are junk, and transposons are junk. I have already stated that I diasgree with PZ on these points [see PZ Myers Talks About Junk DNA]. Now I want to be clear on why Jonathan McLatchie is wrong.
  1. Introns are mostly junk. I think PZ exaggerated a bit when he dismissed all introns as junk. My position is that we should treat introns as functional elements of a gene even though many (but not all) of them could probably be deleted without affecting the survival of the species. Each intron has about 50-80 bp of essential information that's required for proper splicing [Junk in Your Genome: Protein-Encoding Genes]. The rest of the intron, which can be thousand of base pairs in length, is mostly junk [Junk in Your Genome: Intron Size and Distribution]. Some introns contain essential gene regulatory regions and some contain essential genes. That does not mean that all intron sequences are functional.
  2. Telomeres are not junk. I don't think telomeres are junk [Telomeres]. They are absolutely required for proper DNA replication. PZ Myers agrees that telomeres (and centromeres) are functional DNA (28 minutes into the talk). Jonathan McLatchie claims that PZ describes telomeres as junk DNA, "Myers departs from the facts, however, when he asserts that these telomeric repetitive elements are non-functional." McLatchie is not telling the truth.
  3. Defective Transposons are Junk. PZ Myers talks about transposons as mobile genetic elements and states that transposons make up more than half of our genome. That's all junk according to PZ Myers. My position is that the small number of active transposons are functional selfish genes and the real junk is the defective transposon sequences that make up most of the genome [Transposon Insertions in the Human Genome]. Thus, I differ a bit from PZ's position. Jonathan McLatchie, like Jonathan Wells, argues that because the occasional defective transposon in the odd species has acquired a function, this means that most of the defective transposon sequences (~50% of the genome) are functional. This is nonsense.

[Image Credit: The image shows human chromosomes labelled with a telomere probe (yellow), from Christoher Counter at Duke University.]

Monday's Molecule #154

 
Today's molecule is a bit more complicated than some of the others. You have to identify the molecule (common name only) and describe (briefly) its function. Can you name the precursor?

Post your answer in the comments. I'll hold off releasing any comments for 24 hours. The first one with the correct answer wins. I will only post correct answers to avoid embarrassment. This is your last chance to enter the Christmas draw for a free textbook!

There could be two winners. If the first correct answer isn't from an undergraduate student then I'll select a second winner from those undergraduates who post the correct answer. You will need to identify yourself as an undergraduate in order to win. (Put "undergraduate" at the bottom of your comment.) Every undergraduate who posts a correct answer will have their names entered in a Christmas draw. The winner gets a free autographed copy of my book! (One entry per week. If you post a correct answer every week you will have ten chances to win.)

Some past winners are from distant lands so their chances of taking up my offer of a free lunch are slim. (That's why I can afford to do this!)

In order to win you must post your correct name. Anonymous and pseudoanonymous commenters can't win the free lunch.

Winners will have to contact me by email to arrange a lunch date.

UPDATE: The molecule is thyrotropin-releasing hormone. It's derived from a long precursor protein containing multiple repeats of the tripeptide Glu-His-Pro.

The winner is Joseph C. Somody.

I'll announce the undergraduate winner of my textbook on Christmas day.

Winners
Nov. 2009: Jason Oakley, Alex Ling
Oct. 17: Bill Chaney, Roger Fan
Oct. 24: DK
Oct. 31: Joseph C. Somody
Nov. 7: Jason Oakley
Nov. 15: Thomas Ferraro, Vipulan Vigneswaran
Nov. 21: Vipulan Vigneswaran (honorary mention to Raul A. Félix de Sousa)
Nov. 28: Philip Rodger
Dec. 5: 凌嘉誠 (Alex Ling)
Dec. 12: Bill Chaney


Friday, December 16, 2011

Key Figures in Intelligent Design Creationism

 
Here's a recording of interviews with three prominent Intelligent Design Creationists ....

Guillermo Gonzalez is a Senior Fellow at the Center for Science and Culture (Discovery Institute).
Douglas Axe, director of The Biologic Institute, which is largely funded by the Discovery Institute.
David Berlinski is a Senior Fellow at the Center for Science and Culture (Discovery Institute).

This is the best they have to offer. It gives you a very good idea of what Intelligent Design Creationism is all about. It's about nothing ... there's not a single mention of what IDC stands for and not a single bit of evidence for the existence of a designer. All you hear is whining about real science (evolution) and conspiracies.

Here's a quotation from Berlinski.
Nobody else is doing what the Discovery Institute has been able to do, and that is really put an entire scientific establishment on the defensive, forced for the first time to respond to some very significant criticism...




Christopher Hitchens (1949 - 2011 )

 
Christopher Hitchens died yesterday and everyone in the atheist community is going to pay tribute in their own special way. For me, the highlight of Hitchen's career was last year's debate with Tony Blair here in Toronto (Nov. 26, 2010). The subject was "Is religion a force for good or ill?"

This is his opening statement.